Involvement of the corpus callosum secondary to various conditions leading to cytotoxic edema has been defined as “Cytotoxic lesions of the corpus callosum (CLOCCs)”. These lesions are mostly associated with… Click to show full abstract
Involvement of the corpus callosum secondary to various conditions leading to cytotoxic edema has been defined as “Cytotoxic lesions of the corpus callosum (CLOCCs)”. These lesions are mostly associated with encephalitis, chronic alcoholism, malignancy, trauma, subarachnoid hemorrhage, metabolic disorders, antiepileptic drug toxicity or withdrawal, infection and various other causes [1]. This distinctive clinicoradiological entity usually presents with altered consciousness and seizures but presentation with callosal disconnection syndrome has not been described. Clinical outcome is reported to be favorable in most patients with complete recovery, unless there is a severe underlying disorder. Although the pathophysiologic mechanism is not completely understood, release of cytokines is considered as the initiator of the cascade producing the cytotoxic lesions. Corpus callosum, particularly the splenium, is the typical brain region vulnerable to this cytokinopathy [1]. We present a metronidazole-induced CLOCCs case with poor prognosis, manifesting an extensive callosal lesion extending into the extracallosal (more lateral) white matter fibers.
               
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